Cases reported "Graves Disease"

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441/879. Localized myxedema on the nasal dorsum in a patient with Graves' disease: report of a case.

    We report the case of a 56-year-old Japanese female with Graves' disease associated with localized myxedema on the nasal dorsum. The patient developed localized myxedema concomitantly with hyperthyroidism before antithyroid therapy was given. The lesion was totally removed surgically, as it was small and well circumscribed. Although unusual locations of localized myxedema have been reported elsewhere, there is to date no case of localized myxedema on the nasal dorsum without involvement of the pretibial area reported in the literature. We discuss this unique feature of our patient. ( info)

442/879. Primary hyperthyroidism occurring in association with acromegaly.

    Two patients with acromegaly who also developed primary hyperthyroidism are described. One case presented de novo with Graves' disease and acromegaly and the other developed hyperthyroidism several years after the diagnosis of acromegaly had been made. No associated adenomas could be demonstrated. The association between acromegaly and thyroid disease is discussed. ( info)

443/879. Persistence of low serum thyroid hormone levels in a Graves' disease patient receiving supraphysiologic L-thyroxine replacement therapy.

    A patient with Graves' disease was treated with radioactive iodine. For several years following treatment, the patient displayed clinical hypothyroidism and persistently low serum thyroxine (T4) and triiodothyronine (T3) levels despite large T4 replacement dosage (0.3-0.4 mg L-thyroxine daily). A defect in T4 absorption was considered unlikely since absorption of fat soluble materials (vitamins A and E) was essentially normal as reflected by their serum concentrations. Abnormalities in serum protein binding of T4 especially by immunoglobulins were suspected; however, thyroid hormone binding antibodies were absent. thyroxine binding prealbumin (TBPA) levels were either frankly elevated or in the upper normal range and such variations were mirrored by retinol binding protein (RBP) concentrations. thyroxine binding globulin (TBG) concentration was normal. A surprising finding was an elevated percent dialyzable thyroxine (.041%; normal range, .018-.034%) in spite of a normal concentration of TBG. serum free fatty acid levels were also elevated. The marked increase in percent free T4 (FT4) fraction together with a low serum total T4 concentration resulted in normal or marginally elevated FT4 levels. An increase in T4 metabolic clearance as suggested by the elevated percent FT4 fraction was corroborated by steady state serum T4 values observed following changes in T4 dosage.(ABSTRACT TRUNCATED AT 250 WORDS) ( info)

444/879. A case of Graves' disease associated with polymyositis.

    A patient with Graves' disease associated with severe muscle weakness who was finally diagnosed as polymyositis by pathological examination of the muscle is reported. A 28-year-old women was incidentally found to have hyperthyroidism when she consulted a hospital for the evaluation and treatment of anemia in 1979. She was treated with methimazole for approximately a month when she stopped the medication by herself. Approximately two yr later (Nov. 4, 1981) she consulted another hospital with complaints of palpitation and muscle weakness. diagnosis of hyperthyroidism due to Graves' disease and thyrotoxic myopathy were made, followed by the treatment with radioiodine (4 mCi of 131I). She was further treated with propylthiouracil (PTU). Four yr after the treatment, serum thyroid hormone concentration declined to the lower level than normal and serum TSH concentration increased. She was subsequently treated with synthetic I-T4. Despite the fact she became euthyroid with the treatment, muscle weakness as well as elevated concentrations of muscle enzymes were not improved. Muscle biopsy was made in July 1983, and she was diagnosed as immune polymyositis and treatment with prednisolone and cyclophosphamide in addition to PTU or I-T4, was started. With the treatment, serum LDH decreased to the normal range. However she still has muscle weakness and serum concentrations of CPK and aldolase are still in higher levels than normal range. ( info)

445/879. Thyrotoxic hyperemesis: a case report.

    A male patient with hyperemesis as a result of hyperthyroidism was presented. Investigations for causes were negative except for hyperthyroxinaemia. Treatment with antithyroid drug relieved the symptom. Hyperemesis associated with hyperthyroidism occurs predominantly in females. A likely emetic factor oestrogen. hyperthyroidism could have potentiated this effect. Levels of oestrogens are raised in thyrotoxicosis. The hyperthyroidism, the raised oestrogens and a low emetic threshold conspired to hyperemesis in this patient, a situation not unlike hyperemesis gravidarum. Thyrotoxic vomiting once recognised is readily by antithyroid treatment. ( info)

446/879. Increased muscle tension and reduced elasticity of affected muscles in recent-onset Graves' disease caused primarily by active muscle contraction.

    In 3 patients with Graves' disease of recent onset, length-tension diagrams were made during surgery for squint under eyedrop anesthesia. The affected muscles were found to be very stiff when the other eye looked straight ahead. It was expected that these stiff muscles would be able to shorten to some extent but would be unable to lengthen, due to fibrosis of the muscle. We found that the affected muscles did not shorten very much when the other eye looked into the field of action of the muscle. Unexpectedly however, they lengthened considerably when the other eye looked out of the field of action of the muscle. This finding implies that the raised muscle tension and reduced elasticity of affected muscles in these cases of Graves' disease of recent onset were primarily caused by active muscle contraction, not by fibrosis. ( info)

447/879. Hypokalaemic, hypophosphatemic thyrotoxic periodic paralysis.

    Thyrotoxic periodic paralysis is an uncommon neuromuscular disorder frequently associated with severe hypokalemia. We describe a patient with hypophosphatemia occurring in the setting of hypokalemic thyrotoxic periodic paralysis, an association reported only once previously. A review of the literature indicates that this combined biochemical derangement may not be uncommon and that thyrotoxic periodic paralysis should be recognized as a potential cause of hypophosphatemia. The correction of both hypokalemia and hypophosphatemia may lead to a more rapid resolution of the associated acute neurologic syndrome. ( info)

448/879. carbimazole-induced acute cholestatic hepatitis.

    A case of carbimazole-induced cholestatic hepatitis is presented. A woman received carbimazole for hyperthyroidism for 3 months. Five months later, she had prompt recurrence of cholestasis parameters after rechallenge (2 days of treatment). Histologic examination showed predominantly centrilobular cholestasis. Only 5 other cases have been published in the literature. An idiosyncratic mechanism seems likely. ( info)

449/879. Hyperglucagonemia of insulin autoimmune syndrome induced by methimazole in a patient with Graves' disease.

    A 47-year-old man with Graves' disease suffered from a feeling of hunger and sweating in the night, polyarthralgia and fever one month after the start of treatment with methimazole. The above symptoms were ascribed to the side effects of methimazole; insulin autoimmune syndrome and lupus-like syndrome. The change in the antithyroid drug to propylthiouracil caused an amelioration of the symptoms. In addition to an anti-insulin antibody with a high binding capacity, hyperglucagonemia (260 pg/ml with a plasma glucose level of 61 mg/dl) was observed, which returned to normal in parallel with the decrease in the insulin binding capacity of the plasma one month after beginning the treatment with propylthiouracil. A normal decrease in the plasma glucagon level due to exogenous insulin (2 mU/kg/min) was observed with the euglycemic clamp. However, the plasma glucagon level was not suppressed by the oral glucose loading and elicited a poor response to the arginine infusion. Taking previous reports into account, this basal hyperglucagonemia seems to be a characteristic finding in the insulin autoimmune syndrome, while a sluggish response of glucagon to oral glucose or arginine infusion might be ascribed to hyperthyroidism. This is the first case report concerning a kinetical study of the glucagon secretion in insulin autoimmune syndrome with Graves' disease. ( info)

450/879. Medullary thyroid cancer and Graves' disease.

    A focus of medullary thyroid cancer was found at frozen section analysis of tissue from a patient with Graves' disease undergoing thyroid lobectomy. An increased incidence of papillary-follicular thyroid cancer has been noted in Graves' disease. This report describes the unique association of medullary thyroid cancer and Graves' disease. ( info)
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